Resistance to Blood Flow
Resistance to blood flow within a vascular network is determined by the size of individual vessels (length and diameter), the organization of the vascular network (series and parallel arrangements), physical characteristics of the blood (viscosity), flow behavior (laminar vs turbulent flow; steady vs pulsatile flow), and extravascular mechanical forces acting upon the vasculature.
Of the above factors, changes in vessel diameter are most important quantitatively for regulating blood flow within an organ, as well as for regulating arterial pressure. Changes in vessel diameter, particularly in small arteries and arterioles, enable organs to adjust their own blood flow to meet the metabolic requirements of the tissue. Therefore, if an organ needs to adjust its blood flow (and therefore, oxygen delivery), cells surrounding these blood vessels release vasoactive substances that can either constrict or dilate the resistance vessels.
The ability of an organ to regulate its own blood flow is termed local regulation of blood flow and is mediated by vasoconstrictor and vasodilator substances released by the tissue surrounding blood vessels (vasoactive metabolites) and by the vascular endothelium. There is also a mechanism intrinsic to the vascular smooth muscle (myogenic mechanism) that is involved in local blood flow regulation.
In organs such as the heart and skeletal muscle, mechanical activity (contraction and relaxation) produces compressive forces that can effectively squeeze vessels within the muscular wall, decreasing vessel diameters and increasing resistance to flow during muscle contraction (see extravascular compression).
Besides local regulatory mechanisms, there are extrinsic mechanisms acting on the vasculature to regulate vessel diameter. One important extrinsic mechanism regulating vascular diameter operates through the autonomic nerve innervation of blood vessels. Sympathetic adrenergic influences acting through vascular alpha-adrenoceptors cause resistance vessels and veins to be partially constricted under basal conditions. This is termed "sympathetic vascular tone." Therefore, removal of sympathetic adrenergic influences (for example, by administration of an alpha-adrenoceptor antagonist or by sympathectomy) leads to vasodilation and an increase in organ blood flow. A second type of extrinsic influence on the vasculature is circulating vasoactive hormones such as angiotensin II, epinephrine and norepinephrine, vasopressin (antidiuretic hormone, ADH), atrial natriuretic peptide (ANP), and endothelin. The neural and humoral factors, while affecting organ blood flow, primarily serve the function of regulating arterial pressure by altering systemic vascular resistance.